This is a competing continuation proposal for a project which is studying how fatigue damage in cortical bone depends on the applied stress range and the number of cycles applied. We are interested in both microcrack damage and damage in the form of diminished mechanical properties. We have also developed a mechanistic theoretical model for relating these two kinds of damage. This model has been successful in predicting fatigue life and reduction of modulus as a function of the number of cycles applied, N. The theory is based on the concept that osteonal bone is a fiber-matrix composite in which secondary osteons are the fibers and primary tissue and osteon fragments are the matrix. It is also based on the observation that different kinds of matrix and fiber damage occur when human cortical bone is loaded in tension and compression. The resulting fiber-matrix damage theory successfully models the E vs. N curves of Pattin et al. (1996) for uniaxial tension and compression of human femoral bone and we have preliminary validation data for flexural fatigue of human femoral bone as well. Originally, we proposed to use fatigue in four-point bending of specimens machined from equine third metacarpal bones as our experimental model, and this is what we have studied, for the most part, during the first grant period. However, we have found that the equine bone does not exhibit the same kinds of microcrack damage as human cortical bone. Therefore, we propose to shift our emphasis to human femoral bone during the next grant period. Our goals for this work are to rigorously test, and to extend, the fiber-matrix damage theory through a program of experimentation in concert with continued analytical development. In particular, we want to more fully develop the theory in terms of shear stress damage, local variations in bone structure, and bimodal modes of loading.